کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3057127 1186590 2007 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Neurokinins enhance excitability in capsaicin-responsive DRG neurons
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
پیش نمایش صفحه اول مقاله
Neurokinins enhance excitability in capsaicin-responsive DRG neurons
چکیده انگلیسی

Neurokinins released by capsaicin-responsive (C-R) dorsal root ganglia neurons (DRG) may control firing in these neurons by an autofeedback mechanism. Here we used patch clamp techniques to examine the effects of neurokinins on firing properties of dissociated DRG neurons of male rats. In C-R neurons that generated only a few action potentials (APs, termed phasic) in response to long depolarizing current pulses (600 ms), substance P (SP, 0.5 μM) lowered the AP threshold by 11.0 ± 0.3 mV and increased firing from 1.1 ± 0.7 APs to 5.2 ± 0.6 APs. In C-R tonic neurons that fire multiple APs, SP elicited smaller changes in AP threshold (6.0 ± 0.1 mV reduction) and the number of APs (11 ± 1 vs. 9 ± 1 in control). The effects of SP were similar to the effect of heteropodatoxin II (0.05 μM) or low concentrations of 4-aminopyridine (50 μM) that block A-type K+ currents. A selective NK2 agonist, [βAla8]-neurokinin A (4–10) (0.5 μM), mimicked the effects of SP. The effects of SP in C-R phasic neurons were fully reversed by an NK2 receptor antagonist (MEN10376, 0.5 μM) but only partially by a protein kinase C (PKC) inhibitor (bisindolylmaleimide, 0.5 μM). An NK3-selective agonist ([MePhe7]-neurokinin B, 0.5 μM), an NK1-selective agonist ([Sar9, Met11]-substance P, 0.5 μM) or activation of PKC with phorbol 12,13-dibutyrate (0.5 μM) did not change firing. Our data suggest that the excitability of C-R phasic afferent neurons is increased by activation of NK2 receptors and intracellular signaling mediated only in part by PKC.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 205, Issue 1, May 2007, Pages 92–100
نویسندگان
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